Fetal and infant growth and impaired glucose tolerance at age 64
Open accessAbstract
OBJECTIVE: To discover whether reduced fetal and infant growth is associated with non-insulin dependent diabetes and impaired glucose tolerance in adult life. DESIGN: Follow up study of men born during 1920-30 whose birth weights and weights at 1 year were known. SETTING: Hertfordshire, England. SUBJECTS: 468 men born in east Hertfordshire and still living there. MAIN OUTCOME MEASURES: Fasting plasma glucose, insulin, proinsulin, and 32-33 split pro-insulin concentrations and plasma glucose and insulin concentrations 30 and 120 minutes after a 75 g glucose drink. RESULTS: 93 men had impaired glucose tolerance or hitherto undiagnosed diabetes. They had had a lower mean birth weight and a lower weight at 1 year. The proportion of men with impaired glucose tolerance fell progressively from 26% (6/23) among those who had weighted 18 lb (8.16 kg) or less at 1 year to 13% (3/24) among those who had weighed 27 lb (12.25 kg) or more. Corresponding figures for diabetes were 17% (4/23) and nil (0/24). Plasma glucose concentrations at 30 and 120 minutes fell with increasing birth weight and weight at 1 year. Plasma 32-33 split proinsulin concentration fell with increasing weight at 1 year. All these trends were significant and independent of current body mass. Blood pressure was inversely related to birth weight and strongly related to plasma glucose and 32-33 split proinsulin concentrations. CONCLUSIONS: Reduced growth in early life is strongly linked with impaired glucose tolerance and non-insulin dependent diabetes. Reduced early growth is also related to a raised plasma concentration of 32-33 split proinsulin, which is interpreted as a sign of beta cell dysfunction. Reduced intrauterine growth is linked with high blood pressure, which may explain the association between hypertension and impaired glucose tolerance.
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The association between maternal diabetes mellitus and offspring diabetes mellitus is not solely genetic, as inferred from lower diabetes rates in offspring born before their mothers developed diabetes, including among sibling pairs whose birth dates straddle maternal diabetes onset.
“That this is not simply a genetic predisposition is inferred from the finding of lower rates of DM in offspring of women who were born before their mothers developed DM1412; this is true among sibling pairs whose birth dates straddle the onset of their mother’s DM.1409”
From American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update. (2022) · cites this paper as [1409]
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMaternal diabetes mellitus is one of the strongest risk factors for development of type 2 diabetes among children.
“Maternal DM is one of the strongest risk factors for the development of T2D among children.1409–1411”
From American Association of Clinical Endocrinology Clinical Practice Guideline: Developing a Diabetes Mellitus Comprehensive Care Plan-2022 Update. (2022) · cites this paper as [1409]
The Discussion (page not available) says diabetes during pregnancy leads to fetal beta-cell hyperplasia, but does not say it increases children’s risk of type 2 diabetes. The study reports an association between reduced fetal and infant growth and impaired glucose tolerance in men aged 59–70; searches for maternal diabetes as a risk factor for children’s type 2 diabetes found no supporting passage. (LLM, conf=0.76)
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Long-Term Effects of Placental Growth on Overweight and Body Composition
Eriksson, J. G., Gelow, J., Thornburg, K. L., Osmond, C., Laakso, M., Uusitupa, M., Lindi, V., Kajantie, E., & Barker, D. J. P. (2012) · International Journal of Pediatrics · doi:10.1155/2012/324185 · Cited by 14 · see citing works
Self-citationKhurana, I., Kaspi, A., Ziemann, M., Block, T., Connor, T., Spolding, B., Cooper, A., Zimmet, P., El-Osta, A., & Walder, K. (2016) · International Journal of Obesity · doi:10.1038/ijo.2016.64 · Cited by 11 · see citing works
- Authors
- Hales, C. N., Barker, D. J., Clark, P. M., Cox, L. J., Fall, C., Osmond, C., & Winter, P. D.
- Affiliations
- University of Cambridge (GB)
- Venue
- BMJ
- Publisher
- BMJ
- Published
- 1991-10-26
- Volume
- 303
- Issue
- 6809
- Pages
- 1019-1022
- ISSN
- 0007-1447 (ISSN-L)
- 0959-8138
- 1468-5833
- OpenAlex
- W2031792984
- Cited by
- 2,708
- References
- 22
- Citations by year
- 2026: 14 · 2025: 29 · 2024: 48 · 2023: 37 · 2022: 60 · 2021: 81 · 2020: 66 · 2019: 86 · 2018: 106 · 2017: 92 · 2016: 94 · 2015: 98 · 2014: 111 · 2013: 115 · 2012: 122
- FWCI
- 58.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- BMJ (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- Dunhill Medical Trust
- Wessex Medical Research
- Medical Research Council
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- fetal growth restriction, infant growth, birth weight, impaired glucose tolerance, type 2 diabetes, proinsulin, beta-cell dysfunction, fasting blood glucose, insulin, blood pressure, hypertension, early life growth
- MeSH terms
- Aged, Birth Weight, Blood Glucose, Blood Pressure, Body Weight, Diabetes Mellitus, Type 2, Female, Fetal Growth Retardation, Glucose Tolerance Test, Humans, Insulin, Male, Middle Aged, Pregnancy, Proinsulin, Body Mass Index
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